Experimental Exposure of Pigs to Infectious
Bovine Rhinotracheitis (IBR) Virus*
George T. Woods, R. C. Meyer, and Joseph Simon
SUMMARY
Thirteen specific-pathogen-free pigs were
used in an experiment to determine the patho-
genicity of IBR virus for pigs. Three pigs were
used as controls, eight were exposed to IBR
virus by either the intravenous, subcutaneous,
intratracheal, or intranasal route, and two pigs
served as contact controls. The clinical re-
sponse consisted of a temperature rise, depres-
sion and variable lymphocytosis. The major
tissue alterations were interstitial pneumonitis,
and peribronchiolitis with round cell aggre-
gates and giant cell formation. IBR virus was
not recovered from any of the pigs. A serologic
response was detected in only the pig injected
intravenously.
INTRODUCTION
Infectious bovine rhinotracheitis (IBR)
virus frequently infects cattle. Prior re-
ports have indicated that horses, swine and
sheep are refractory to infection (1) while
there are conflicts in reports of infection
of goats (1, 3, 7). Besides growth in bovine
cell cultures the virus has been propagated
and modified in cultured cells of porcine
origin (6) and others.
Since swine are maintained with feeder
cattle in some Illinois feedlots, and since
various herpes viruses have a wide host
range, additional study of the suscepti-
bility of swine to IBR virus seemed de-
sirable. The following report describes the
*University of Illinois College of Veterinary Medicine,
Department of Pathology and Hygiene and Agricultural
Experiment Station. This work was supported in part
by funds from the Experiment Station and U.S. Public
Health Service General Research Support.
480
results of exposure of pigs by the intra-
venous, subcutaneous, intranasal, and in-
tratracheal routes and by pen contact to
the IBR virus.
MATERIALS AND METHODS
EXPERIMENTAL PIGS: Thirteen crossbred
pigs, eight weeks old, were purchased from
a nationally accredited specific-pathogen-
free herd in Illinois. Three pigs were
placed in an isolation room as controls,
eight were exposed to IBR virus, the re-
maining two were uninoculated contact con-
trols.
SOURCE OF VIRUS: The IBR virus used*
was a strain originally obtained from Dr.
Delbert McKercher of Davis, California.
At Abbott Laboratories, the virus was
passed once in bovine kidney tissue cul-
ture, 4 times in porcine kidney tissue cul-
ture, and then once again in bovine kidney
tissue culture. After the virus reached the
College of Veterinary Medicine it was
passed once in the established bovine kid-
ney cell line of Madin and Darby (MDBK)4
and once in primary porcine kidney cells.
An inoculum of 1 cc was used containing
8 x 106 plaque forming units (PFU) when
titrated on the MDBK cell system.
Serum neutralization tests were con-
ducted as previously described (5).
INOCULATIONS: One pig was inoculated
intravenously (i.v.), another subcutaneous-
ly (s.c), two intratracheally (i.t.) and four
intranasally (i.n.). The three pigs inocu-
lated intranasally were anesthetized with
*Courtesy of Dr. J. C. Holper, Lab. of Inf. Diseases,
Abbott Laboratories, North Chicago, Illinois.
Can. J. comp. Med.
TABLE 1. Routes of Exposure of Pigs to IBR of the study and another at its termina-
Virus and Results of Microscopic Pathologic tion, 12 days later. The exposed pigs were
Examinations of Lungs. necropsied 6, 10 and 12 days post-exposure
(Table 1). Rectal temperatures of the ex-
Days posed pigs were taken daily except on the
Following 11th day post-exposure. The pigs were ob-
Pig Route of Exposure Microscopic served daily for any signs of reaction to
to
No. Exposure Necropsy Pathology the virus.
77 Control 0 Mild interstitial
pneumonitis and
peribronchiolitis RESU LTS
85 Intranasal 6 Mild interstitial Exposed pigs had rectal temperatures of
pneumonitis and 104 F or higher on the fourth, sixth and
peribronchiolitis
seventh days post-infection. The maximal
83 Intranasal 6 Mild interstitial temperature, 105.0 F, was recorded on the
pneumonitis and sixth day in a pig (No. 85) exposed in-
peribronchiolitis tranasally. In general, the temperature rise
84 Intratracheal 6 Mild interstitial was accompanied by depression. At necrop-
pneumonitis and sy the most extensive change was lung
peribronchiolitis congestion (Fig. 1). Slight turbinate
88 Intravenous 10 Round cell atrophy was observed in pig 85 which had
aggregates* been infected intranasally and necropsied
7 days later. The clinical response and
79 Intratracheal 10 Round cell histologic findings in the exposed and con-
aggregates*
tact control pigs were similar. Lymphocyte
81 Intranasal 10 Round cell counts ranged from 45 to 96%, compared
aggregates* to 66 % in the control killed at the end
78 Control 12 Mild interstitial of the observation. No gross evidence of
penumonitis and tracheitis was observed, but 3 pigs had
peribronchiolitis increased accumulation of mucus in the
trachea and bronchii.
82 Subcutaneous 12 Round cell
aggregates* The major tissue changes occurred in
83 Intranasal 12 Slight interstitial the lungs and included interstitial pneu-
pneumonitis and monitis, peribronchiolitis, round cell ag-
peribronchiolitis gregates, with giant cell formation and
86 Contact
epithelization (fig. 2 & 3). Four pigs that
Control 12 Round cell were exposed i.n. and i.t. had greater quan-
aggregates* tities of inflammatory exudate in the tur-
binates than did the controls. Cytopa-
*Lungs also exhibited slight to marked interstitial thogenic agents were not recovered from
pneumonitis and peribronchiolitis. netropsy specimens nor was any latent

ether prior to inoculation. The remainder

were lightly anesthetized by intravenous
administration of Diabuthal.*
COLLECTION OF SPECIMENS: Serum, ox-
alated blood samples, and a swab of nasal
mucus were collected from each pig ne-
cropsied. Aliquots of lung, kidney, spleen,
liver, heart, turbinates, and trachea were
cultured for microbiol agents as previous-
ly described (8) and others were placed in ....... Ij.;

10% formalin for histologic examination.

A control pig was necropsied at the start
Fig. 1. Marked congestion of apical lobe of lung from
pig exposed to IBR virus intranasally and necropsied
*Diamond Labs., Des Moines, Iowa. 7 days post-exposure.

Vol. 32 - July, 1968 481


al
Fig. 2. Lung from control pig (X 254) with increased
interstitial cellularity.
virus encountered in tissue cultures de-
rived from the kidneys taken from the
pre-exposure control killed at the start of
the experiment.
Hemophilus suis was obtained from the
nasal swabs of two pigs -. one of the con-
trols and one of two principals exposed to
IBR intratracheally No Mycoplasma spp.
were recovered from any of the cultured
lungs, nasal swabs, or tracheas.
The only serologic response developed in
the animal injected intravenously with
IBR virus. It developed neutralizing anti-
body titer of 1:4.
DISCUSSION
IBR virus did not produce overt disease
in the pigs of this study, but produced sys-
temic reactions characterized by tempera-
ture rise, depression, lymphocytosis, and
sero-conversion in 1 animal. IBR virus was
not recovered from any of the pigs; how-
ever, based on clinical and pathologic evi-
dence the virus apparently spread from ex-
posed pigs to contact controls. The his-
tologic response of the lung was similar
to and somewhat characteristic of that as-
cribed to "virus pig pneumonia". (5) How-
ever, gross evidence of pneumonia was ob-
served in only one exposed pig.
Giant cell formation is noteworthy and
may be ascribed to the inflammatory re-
sponse characteristic of the herpes virus
(IBR) used. In the absence of detectable
virus, bacteria, or Mycoplasma sp. from
the lungs, it seems logical to ascribe the
giant cell formation observed on the lung
of exposed pigs as caused by the impact
of the IBR virus.
482
F8iIn
dtn
rcontactpitn
control
"A
cropsied 12 days post-exposure. Interstitial pneumonitis,
peribronchiolitis with round-cell aggregates and giant
cell formation are present. (Top: X 64; bottom: X 254).
ACKNOWL-EDGEMENTS
The technical assistance of Carolyn
Pillai and Charles Campbell is acknowl-
edged.
REFERENCES
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